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10.1038/onc.2012.58 http://scihub22266oqcxt.onion/10.1038/onc.2012.58 22370643!7580497!22370643     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22370643&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Oncogene 2013 ; 32 (3): 296-306 Nephropedia Template TP {{tp|p=22370643|t=2013. MiR-1 and miR-200 inhibit EMT via Slug-dependent and tumorigenesis via Slug-independent mechanisms |pdf=|usr=}}{{22370643}} gab.com Text MiR-1 and miR-200 inhibit EMT via Slug-dependent and tumorigenesis via Slug-independent mechanisms JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=22370643 #FOAvip Epithelial-mesenchymal transition (EMT) is a developmental program of signaling pathways that determine commitment to epithelial and mesenchymal phenotypes. In the prostate, EMT processes have been implicated in benign prostatic hyperplasia and prostate cancer progression. In a model of Pten- and TP53-null prostate adenocarcinoma that progresses via transforming growth factor beta-induced EMT, mesenchymal transformation is characterized by plasticity, leading to various mesenchymal lineages and the production of bone. Here we show that SLUG is a major regulator of mesenchymal differentiation. As microRNAs (miRs) are pleiotropic regulators of differentiation and tumorigenesis, we evaluated miR expression associated with tumorigenesis and EMT. Mir-1 and miR-200 were reduced with progression of prostate adenocarcinoma, and we identify Slug as one of the phylogenetically conserved targets of these miRs. We demonstrate that SLUG is a direct repressor of miR-1 and miR-200 transcription. Thus, SLUG and miR-1/miR-200 act in a self-reinforcing regulatory loop, leading to amplification of EMT. Depletion of Slug inhibited EMT during tumorigenesis, whereas forced expression of miR-1 or miR-200 inhibited both EMT and tumorigenesis in human and mouse model systems. Various miR targets were analyzed, and our findings suggest that miR-1 has roles in regulating EMT and mesenchymal differentiation through Slug and functions in tumor-suppressive programs by regulating additional targets. Twit Text FOAVip MiR-1 and miR-200 inhibit EMT via Slug-dependent and tumorigenesis via Slug-independent mechanisms ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=22370643 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22370643 #FOAvip English Wikipedia <ref>{{Cite pmid|22370643}}</ref> MiR-1 and miR-200 inhibit EMT via Slug-dependent and tumorigenesis via Slug-independent mechanisms #MMPMID22370643 Liu YN; Yin JJ; Abou-Kheir W; Hynes PG; Casey OM; Fang L; Yi M; Stephens RM; Seng V; Sheppard-Tillman H; Martin P; Kelly K Oncogene 2013[Jan]; 32 (3): 296-306 PMID22370643show ga Epithelial-mesenchymal transition (EMT) is a developmental program of signaling pathways that determine commitment to epithelial and mesenchymal phenotypes. In the prostate, EMT processes have been implicated in benign prostatic hyperplasia and prostate cancer progression. In a model of Pten- and TP53-null prostate adenocarcinoma that progresses via transforming growth factor beta-induced EMT, mesenchymal transformation is characterized by plasticity, leading to various mesenchymal lineages and the production of bone. Here we show that SLUG is a major regulator of mesenchymal differentiation. As microRNAs (miRs) are pleiotropic regulators of differentiation and tumorigenesis, we evaluated miR expression associated with tumorigenesis and EMT. Mir-1 and miR-200 were reduced with progression of prostate adenocarcinoma, and we identify Slug as one of the phylogenetically conserved targets of these miRs. We demonstrate that SLUG is a direct repressor of miR-1 and miR-200 transcription. Thus, SLUG and miR-1/miR-200 act in a self-reinforcing regulatory loop, leading to amplification of EMT. Depletion of Slug inhibited EMT during tumorigenesis, whereas forced expression of miR-1 or miR-200 inhibited both EMT and tumorigenesis in human and mouse model systems. Various miR targets were analyzed, and our findings suggest that miR-1 has roles in regulating EMT and mesenchymal differentiation through Slug and functions in tumor-suppressive programs by regulating additional targets. |Adenocarcinoma/genetics/metabolism/*pathology/physiopathology[MESH] |Animals[MESH] |Cell Differentiation/drug effects/genetics[MESH] |Cell Line, Tumor[MESH] |Epithelial-Mesenchymal Transition/drug effects/*genetics[MESH] |Feedback, Physiological/drug effects[MESH] |Gene Expression Regulation, Neoplastic/drug effects/genetics[MESH] |Humans[MESH] |Male[MESH] |Mesenchymal Stem Cells/drug effects/pathology[MESH] |Mice[MESH] |MicroRNAs/*genetics[MESH] |PTEN Phosphohydrolase/deficiency[MESH] |Prostatic Neoplasms/genetics/metabolism/*pathology/physiopathology[MESH] |Snail Family Transcription Factors[MESH] |Transcription Factors/*metabolism[MESH] |Transforming Growth Factor beta/pharmacology[MESH]MiR-1 and miR-200 inhibit EMT via Slug-dependent and tumorigenesis via(epmc).pdf DeepDyve Pubget Overpricing